Can hypopituitarism happen during the acute state of head injury?
NICE says No . . .
Below are two extracts from a letter dated 24 March 2014 from NICE’s solicitors DACBeachcroft. This letter is answering Irwin Mitchell’s letter of claim which argues that NICE is behaving irrationally in excluding information about post-traumatic hypopituitarism from its head injury guideline. NICE’s riposte is that the guideline covers the acute stage only, that hypopituitarism takes months to develop, and therefore has no place in the guidance. However, they cite no research to support their statement.
“4.1 The Guideline focuses on the immediate management of patients who have suffered head trauma. Hypopituitarism is not present in such patients and is therefore not diagnosable.”
Symptoms of hypopituitarism necessarily do not appear on the timescale covered by the Guideline, or anything close to it. First, the pituitary must suffer harm. Then that harm must lead to a reduction in the production of hormone, which in turn must lead to a reduction in the level of hormone in circulation. Finally that reduction must lead to a medically observable effect. A timescale of months may be expected. This is far outside the timescale for guidance addressed to “emergency departments”.”
But Professor Chris Thompson says Yes . . .
Here is an email dated 13 April 2014 from pituitary specialist Chris Thompson, professor of endocrinology at Beaumont Hospital, Dublin and author of much leading research on post-traumatic hypopituitarism, addressed to Joanna Lane:
Once again NICE have not researched the issue.
It has been known since 1969 (Kornblum and Fisher, 1969) that 35% of patients surviving 12 hours after TBI have evidence of infarction of the pituitary. (Infarction is cell death due to lack of blood supply). This was reinforced in 2007 (Salehi, Brain Injury 2007) by data which showed that there was no sign of infarction in 12 patients who died at the scene of TBI, but in 43% of patients who died within the first seven days, and who were studied at post-mortem.
Our own data has shown that 30% of patients studied at 7-14 days post TBI have evidence of subnormal pituitary function (Agha et al Clin Endo 2004) and more recently, a more comprehensive daily assessment of 100 patients with TBI showed that EIGHTY PERCENT HAD SUBNORMAL CORTISOL LEVELS AT SOME STAGE DURING HOSPITAL ADMISSION (Hannon MJ et al JCEM 2013).
We have also presented data showing significant sequelae of acute pituitary injury, including hyponatraemia, hypoglycaemia and hypotension (Agha et al QJM 2005).
1) There is evidence of structural damage occurring during the first week.
2) There is clear evidence that this leads to pituitary dysfunction.
3) The pituitary dysfunction leads to measurable clinical deficits.
In addition, the long term sequelae are no longer disputed.
It seems that NICE are acting in a deliberately delinquent manner in ignoring expert opinion – I wish you luck with the judicial review.
The Legal Aid Agency chooses to believe NICE . .
Here is an extract from the Legal Aid Agency’s letter dated 14 April 2014 to Irwin Mitchell refusing aid to take NICE to Judicial Review. It is clear that the Agency has accepted NICE’s version uncritically without any independent verification.
3. The guidance that you are seeking to review specifically states that it does not cover rehabilitation or long term care. From the information provided hypopituitarism is not something which is diagnosable within the early stages of a head injury and as such I cannot see that it falls within the remit of this guidance.
When the LAA were sent a copy of Professor Thompson’s email they did not respond.
Finally, here is an email from Sir Andrew Dillon to Joanna Lane dated 2 July 2010 (three years earlier) showing NICE to be well aware that life-threatening complications of hypopituitarism can show their effects during the acute stage of head injury.
Dear Ms lane,
Thank you for your email.
I agree that the systematic review which you cite refers to evidence that the incidence of biochemically identified hypopituitarism is higher in the acute phase. The figure of 80%, which you refer to, is for LH/FSH (gonadotrophins) only, and only in one of the two studies. The rate of ACTH deficiency, which if severe would be the only life threatening complication, is cited as 12%. The clinical significance of these biochemical findings is not clear. The review itself states that: ‘Early posttraumatic pituitary dysfunction can be transient in many cases and conversely, hypopituitarism can evolve over several weeks or months after injury.’
In addition, the abstracts of two papers listed at the end as citing this paper include the following two statements:
‘By applying strict diagnostic criteria to an emergency-department-based cohort of TBI patients, it was shown that anterior pituitary dysfunction is rare (<1%). Routine pituitary screening in unselected patients after TBI is unlikely to be cost-effective.’ van der Eerden et al (2010)
The reported variations in the prevalence rates of hypopituitarism after TBI are in part caused by differences in definitions, endocrine assessments of hypopituitarism, and confounding factors. These methodological issues prohibit simple generalizations of results of original studies on TBI-associated hypopituitarism in the perspective of meta-analyses or reviews.’ Kokshoorn et al (2010).
We do have to take informed decisions the best way to allocate our limited resources and I remain of the view that the best approach to this topic is a clinical guideline which addresses the question as to whether routine screening of patients following traumatic brain injury for pituitary dysfunction is clinically and cost effective.
National Institute for Health and Clinical Excellence
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How, in this day and age, can the patient’s welfare be so callously ignored?